Atrial fibrillation is the most common arrhythmia, affecting two million Americans per year, increasing mortality and morbidity (stroke) with significant economic burden on society. While the conditions predisposing to atrial fibrillation (AF), such as hypertension and cardiovascular disease, are well described, what factors trigger the actual occurrence of an episode of AT are unknown. Emotion, through activation of sympathetic pathways, may trigger episodes of AF. Although groups of patients with "adrenergically-mediated" atrial fibrillation have been described, evidence that emotional stimuli can trigger AF comes only from small case-series. Our prior research has shown that anger can precipitate ventricular arrhythmias in patients with implantable cardioverter-defibrillators (ICDs). In that study, 40% of the small group of shocks received "inappropriately" for AF were precipitated by anger or anxiety. While effects of mental stress on electrical properties of the atrium have not been well described, pharmacological autonomic manipulations can alter atrial electrophysiology, supporting the hypothesis that sympathetic arousal by emotion has the potential to trigger AF. The primary goal of the proposed study is to determine whether emotional factors can trigger episodes of symptomatic atrial fibrillation in patients with symptomatic paroxysmal or persistent AF, using a case-crossover design, in which each patient acts as his own control. We hypothesize that anger and anxiety will precede episodes of AF in patients with paroxysmal or intermittent AF. We also propose to investigate, in a parallel prospective cohort study, whether an individual's emotional reactivity, as measured by response to induced mental stress testing in the laboratory setting, ("mental stress reactivity") and by psychological profile, can predict the likelihood and frequency of AF recurrence, as has been found for other cardiovascular events. We hypothesize that those patients demonstrating greater sympathetic response during mental stress testing, as determined by comprehensive hemodynamic, neuroendocrine, and non-invasive electrophysiological evaluation, will have earlier and more frequent recurrences of AF in follow-up. Further, we hypothesize that patients scoring higher on measures of anger, anxiety, and hostility on psychological testing will have also have a higher propensity to recurrent AF. Determining triggers of AF, and identifying individuals at increased risk of recurrence, may lead to future therapeutic interventions aimed at decreasing the effects of triggers on the individual patient.